Epithelial ingrowth occurs in up to 4.3% of patients following laser-assisted
in situ keratomileusis.1 Treatment varies
from observation to lifting the flap and scraping away the epithelium. With
recurrence, additional treatment options include the use of an excimer laser,
cocaine, proparacaine hydrochloride, or alcohol on the stromal bed and flap
and suturing the abnormal flap edge. Studies on the efficacy of these interventions
are lacking. We report a case of total flap melting following alcohol application
to the interface to treat recurrent epithelial ingrowth.
A 52-year-old woman underwent bilateral laser-assisted in situ keratomileusis
for moderate myopic astigmatism. Postoperatively the patient had irritation
and focal flap edema in her left eye that persisted for 6 months before epithelial
ingrowth was noted. The patient's flap was lifted, scraped, and irrigated
8 months postoperatively. Twelve days later, recurrent epithelial ingrowth
was observed. The retreatment consisted of elevating the flap, scraping the
stromal bed and flap undersurface, applying absolute alcohol on a 6-mm sponge
to the stromal bed and flap undersurface twice for 10 seconds, and irrigating
At the time of referral 6 days later, the patient's visual acuity was
20/200 with pinhole approximation, and she had a large central epithelial
defect. The edematous flap made the interface difficult to examine. Her epithelial
defect improved during the next week with conservative treatment, and her
visual activity improved to 20/80 with pinhole approximation. Four days later,
the patient returned with 80% melting of the flap (Figure 1). The remaining nasal and temporal pieces of the flap were
removed and sent to the pathology department (Figure 2).
Remaining flap attached to nasal
hinge after flap melting.
Hematoxylin-eosin stain of laser-assisted
in situ keratomileusis flap with irregular epithelium (top) and epithelial
ingrowth under the flap (bottom). Note the Bowman layer for orientation.
Many theories exist regarding the source of the epithelial cells in
epithelial ingrowth, but most researchers believe that the cells grow under
the flap from the keratotomyincision. The factors that stimulate or allow
this growth are not known, but poor adhesion of the flap may be an important
factor. When treating epithelial ingrowth, complete removal or death of all
of the cells is important to prevent recurrence. When initial scraping and
irrigating fails, additional measures such as the use of an excimer laser
or alcohol on the stromal bed and flap have been attempted. Alcohol has been
used in photorefractive keratectomy for many years to remove the epithelium.2 However, some reports show that alcohol can induce
keratocyte death and increase inflammation compared with mechanical debridement.3
Use of alcohol in this case may have influenced flap adhesion in several
ways, allowing aggressive epithelial ingrowth to occur with subsequent flap
melting. First, the alcohol may have caused keratocyte death on both the flap
and stroma, which can affect the interaction and wound healing of these 2
surfaces. Second, the alcohol may have inadvertently touched the surface epithelium,
leading to the epithelial defect, flap edema, and poor flap adhesion. Because
there is a lack of basic and clinical research evaluating alcohol in the treatment
of epithelial ingrowth, use of this toxic agent in the lamellar interface
should be approached with caution.
Corresponding author: Carol L. Karp, MD, Bascom Palmer Eye Institute,
900 NW 17th St, Miami, FL 33136.
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